Oxidative stress induced by HIV-1 F34IVpr in Schizosaccharomyces pombe is one of its multiple functions.

Human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) exerts multiple effects on viral and host cellular activities during infection, including induction of cell cycle G(2) arrest and cell death in both human and the fission yeast Schizosaccharomyces pombe cells. In this study, a mutant derivative of Vpr (F34IVpr), which causes transient G2 arrest with little or no effect of cell killing, was used to study the molecular impact of Vpr on cellular oxidative stress responses in S. pombe. We demonstrated here that F34IVpr triggers low level of complex and atypical oxidative stress responses in comparison with its parental strain SP223 in early (14-h) and late (35-h) log phase cultures. Specifically, F34IVpr production in S. pombe causes significantly elevated levels of reactive oxygen species such as superoxide and peroxides; meanwhile, it also induces decreased levels of glutathione, hydroxyl radical concentrations and specific enzyme activities such as those of antioxidant enzymes including superoxide dismutases, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and glutathione transferase. These observations may provide functional insights into the significance of Vpr-induced oxidative stress as part of the multifaceted functions of Vpr, and contribute to the development of future new strategies aimed to reduce the adverse Vpr-mediated effects in HIV-infected patients. Copyright 2009 Elsevier Inc. All rights reserved.